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- W2008227478 abstract "Nonsteroidal anti-inflammatory drugs inhibit cyclo-oxygenase activity and thereby reduce prostaglandin synthesis. Studies in humans have used these cyclo-oxygenase inhibitors to examine the role of prostaglandins in controlling renal function. Although short-term studies have demonstrated reductions in effective renal plasma flow, glomerular filtration rate, urinary sodium excretion, and plasma renin activity, long-term administration of nonsteroidal anti-inflammatory drugs does not result in significant or clinically important changes in renal function in normal human subjects. If healthy volunteers are placed on low-sodium diets or treated with diuretics, both renal hemodynamics and salt and water excretion can become prostaglandin-dependent. Studies in normal subjects suggest that sulindac, a nonsteroidal anti-inflammatory drug that undergoes biotransformation in the kidney, does not inhibit renal prostaglandin synthesis or urinary sodium excretion under basal conditions but may impair furosemide-stimulated prostaglandin synthesis and changes in renal function. Doses of sulindac that spare basal renal cyclo-oxygenase do inhibit extrarenal cyclooxygenase. The mechanism responsible for this biochemical selectivity of sulindac is not related to a differential sensitivity of the renal cyclo-oxygenase to the active metabolite of sulindac, sulindac sulfide. Sulindac sulfide, in concentrations as low as 1 nM, was equipotent to indomethacin as an inhibitor of prostaglandin E2 synthesis in primary cultures of three renal cell lines. Appropriate clinical use of all nonsteroidal anti-inflammatory drugs, including sulindac, requires careful consideration of risk factors that predispose to nephrotoxicity and careful monitoring when administered to patients at risk." @default.
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- W2008227478 date "1986-08-01" @default.
- W2008227478 modified "2023-10-04" @default.
- W2008227478 title "Effects of nonsteroidal anti-inflammatory drugs in healthy subjects" @default.
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- W2008227478 doi "https://doi.org/10.1016/0002-9343(86)90908-3" @default.
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